2022/06/28 更新

写真a

サクラギ シゲオ
櫻木 繁雄
所属
理工学術院 先進理工学部
職名
講師(任期付)

学歴

  • 2010年04月
    -
    2014年09月

    大阪大学大学院   生命機能研究科  

経歴

  • 2022年04月
    -
    継続中

    早稲田大学   理工学術院 先進理工学部   講師(任期付)

  • 2020年04月
    -
    2022年03月

    早稲田大学   理工学術院総合研究所   次席研究員

  • 2018年04月
    -
    2020年03月

    山形大学   医学部 医学科   助教

  • 2016年04月
    -
    2018年03月

    東北大学大学院   生命科学研究科   特任助教

  • 2014年10月
    -
    2016年03月

    名古屋大学大学院   理学研究科   博士研究員

所属学協会

  •  
     
     

    日本生理学会

  •  
     
     

    日本神経科学学会

 

研究分野

  • 生理学

  • 神経科学一般

  • 薬理学

研究キーワード

  • シナプス可塑性

  • 記憶

  • BDNF

  • 海馬

  • アストロサイト

  • 電気生理学

  • 1分子イメージング

  • カルシウムイメージング

  • 光遺伝学

▼全件表示

論文

  • Inhibitory Synaptic Transmission Tuned by Ca2+ and Glutamate Through the Control of GABAAR Lateral Diffusion Dynamics

    Bannai H, Niwa F, Sakuragi S, Mikoshiba K

    Dev. Growth Differ.   62 ( 6 ) 398 - 406  2020年04月  [査読有り]

    DOI

  • Optogenetic study of the response interaction among multi-afferent inputs in the barrel cortex of rats

    Liu Y, Ohshiro T, Sakuragi S, Koizumi K, Mushiake H, Ishizuka T, Yawo H

    Sci. Rep.   9 ( 1 ) 3917  2019年03月  [査読有り]

    DOI

  • Astroglial Ca2+ signaling is generated by the coordination of IP3R and store-operated Ca2+ channels

    Sakuragi S, Niwa F, Oda Y, Mikoshiba K, Bannai H

    Biochem. Biophys. Res. Commun.   486 ( 4 ) 879 - 885  2017年05月  [査読有り]

    担当区分:筆頭著者

     概要を見る

    Astrocytes play key roles in the central nervous system and regulate local blood flow and synaptic transmission via intracellular calcium (Ca2+) signaling. Astrocytic Ca2+ signals are generated by multiple pathways: Ca2+ release from the endoplasmic reticulum (ER) via the inositol 1, 4, 5-trisphosphate receptor (IP3R) and Ca2+ influx through various Ca2+ channels on the plasma membrane. However, the Ca2+ channels involved in astrocytic Ca2+ homeostasis or signaling have not been fully characterized. Here, we demonstrate that spontaneous astrocytic Ca2+ transients in cultured hippocampal astrocytes were induced by cooperation between the Ca2+ release from the ER and the Ca2+ influx through store-operated calcium channels (SOCCs) on the plasma membrane. Ca2+ imaging with plasma membrane targeted GCaMP6f revealed that spontaneous astroglial Ca2+ transients were impaired by pharmacological blockade of not only Ca2+ release through IP(3)Rs, but also Ca2+ influx through SOCCs. Loss of SOCC activity resulted in the depletion of ER Ca2+, suggesting that SOCCs are activated without store depletion in hippocampal astrocytes. Our findings indicate that sustained SOCC activity, together with that of the sarco-endoplasmic reticulum Ca2+-ATPase, contribute to the maintenance of astrocytic Ca2+ store levels, ultimately enabling astrocytic Ca2+ signaling. (C) 2017 Elsevier Inc. All rights reserved.

    DOI

  • Kinetic characteristics of chimeric channelrhodopsins implicate the molecular identity involved in desensitization

    Zamani A*, Sakuragi S* (*equal contribution), Ishizuka T, Yawo H

    Biophys. Physicobiol.   14   13 - 22  2017年01月  [査読有り]

    担当区分:筆頭著者

    DOI

  • Dissection of local Ca2+ signals inside cytosol by ER-targeted Ca2+ indicator

    Niwa F, Sakuragi S, Kobayashi A, Takagi S, Oda Y, Bannai H, Mikoshiba K

    Biochem. Biophys. Res. Comm.   479 ( 1 ) 67 - 73  2016年10月  [査読有り]

    DOI

  • Dendritic spine dynamics leading to spine elimination after repeated inductions of LTD

    Sho Hasegawa, Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    SCIENTIFIC REPORTS   5   7707  2015年01月  [査読有り]

     概要を見る

    Memory is fixed solidly by repetition. However, the cellular mechanism underlying this repetition-dependent memory consolidation/reconsolidation remains unclear. In our previous study using stable slice cultures of the rodent hippocampus, we found long-lasting synaptic enhancement/suppression coupled with synapse formation/elimination after repeated inductions of chemical LTP/LTD, respectively. We proposed these phenomena as useful model systems for analyzing repetition-dependent memory consolidation. Recently, we analyzed the dynamics of dendritic spines during development of the enhancement, and found that the spines increased in number following characteristic stochastic processes. The current study investigates spine dynamics during the development of the suppression. We found that the rate of spine retraction increased immediately leaving that of spine generation unaltered. Spine elimination occurred independent of the pre-existing spine density on the dendritic segment. In terms of elimination, mushroom-type spines were not necessarily more stable than stubby-type and thin-type spines.

    DOI

  • Involvement of TrkB- and p75NTR -signaling pathways in two contrasting forms of long-lasting synaptic plasticity

    Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    Scientific Reports   3   3185  2013年  [査読有り]

    担当区分:筆頭著者

     概要を見る

    The repetition of experience is often necessary to establish long-lasting memory. However, the cellular mechanisms underlying this repetition-dependent consolidation of memory remain unclear. We previously observed in organotypic slice cultures of the rodent hippocampus that repeated inductions of long-term potentiation (LTP) led to a slowly developing long-lasting synaptic enhancement coupled with synaptogenesis. We also reported that repeated inductions of long-term depression (LTD) produced a long-lasting synaptic suppression coupled with synapse elimination. We proposed these phenomena as useful in vitro models for analyzing repetition-dependent consolidation. Here, we hypothesized that the enhancement and suppression are mediated by the brain-derived neurotrophic factor (BDNF)-TrkB signaling pathway and the proBDNF-p75 NTR pathway, respectively. When we masked the respective pathways, reversals of the enhancement and suppression resulted. These results suggest the alternative activation of the p75 NTR pathway by BDNF under TrkB-masking conditions and of the TrkB pathway by proBDNF under p75 NTR -masking conditions, thus supporting the aforementioned hypothesis.

    DOI PubMed

  • Involvement of the p75(NTR) Signaling Pathway in Persistent Synaptic Suppression Coupled With Synapse Elimination Following Repeated Long-Term Depression Induction

    Yoshihiro Egashira, Tsunehiro Tanaka, Priyanka Soni, Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    JOURNAL OF NEUROSCIENCE RESEARCH   88 ( 16 ) 3433 - 3446  2010年12月  [査読有り]

     概要を見る

    Synaptic plasticity, especially structural plasticity, is thought to be a basis for long-lasting memory. We previously reported that, in rat hippocampus slice cultures, repeated induction of long-term depression (LTD) by application of a metabotropic glutamate receptor (mGluR) agonist led to slowly developing, long-lasting synaptic suppression coupled with synapse elimination. We referred to this phenomenon as LOSS (LTD-repetition-operated synaptic suppression) to discriminate it from conventional single LTD and proposed it as a model for analyzing structural plasticity. Recently, proneurotrophin-activated p75(NTR) signaling has been gaining attention as a possible pathway for the regulation of both neuronal apoptosis and synaptic plasticity. In this study, we examined whether this signaling has a role in the establishment of LOSS. The application of anisomycin indicated that, for LOSS to occur, novel protein synthesis is needed within 6 hr after the induction of mGluR-dependent LTD, which demonstrates that LOSS is an active process and therefore is not due to withering in response to a shortage of trophic factors. Furthermore, we found that pro-BDNF (a species of proneurotrophins) is newly synthesized within 6 hr after the induction of LTD. We therefore exogenously applied a cleavage-resistant form of pro-BDNF, finding synaptic suppression similar to LOSS. LOSS could be abolished by the application of an antibody that binds to and neutralizes p75(NTR) following repeated LTD induction. These results suggest involvement of the p75(NTR) signaling pathway in the for g-lasting decremental form of synaptic plasticity. (C) 2010 Wiley-Liss, Inc.

    DOI

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受賞

  • 5th Biophysics and Physicobiology Editors' Choice Award

    2018年07月  

講演・口頭発表等

  • DNAを介した量子ドット1分子イメージングによる膜脂質の動態解析

    櫻木繁雄, 片桐太郎, 李銘哲, 坂内博子

    第11回日本生物物理学会関東支部会  

    発表年月: 2022年03月

  • タウオリゴマー光誘導モデル細胞を用いたタウオリゴマーの継時的推移

    櫻木繁雄, 松本弦, 添田義行, 吉村英哲, 高島明彦, 坂内博子

    シンギュラリティ生物学第6回領域会議  

    発表年月: 2022年01月

  • GABAA受容体の拡散運動と配置へのイソフルラン導入の影響

    櫻木繁雄, 小野純一郎, 坂内博子

    第44回日本神経科学大会  

    発表年月: 2021年07月

  • 揮発性麻酔薬による GABAA受容体拡散運動への影響

    櫻木繁雄, 片桐太郎, 小野純一郎, 坂内博子

    日仏生物学会第194回例会  

    発表年月: 2021年06月

  • IP3受容体とストア作動性Ca2+チャネルの協調によるアストロサイトCa2+シグナル誘発機構

    櫻木繁雄, 丹羽史尋, 小田洋一, 坂内博子, 御子柴克彦

    第94回日本生理学会大会   (浜松) 

    発表年月: 2017年03月

  • アストロサイトCa2+シグナルにおけるストア作動性Ca2+チャネルの役割

    櫻木繁雄, 丹羽史尋, 小田洋一, 坂内博子, 御子柴克彦

    第48回東北生理談話会  

    発表年月: 2016年10月

  • Further evidence for the involvement of BDNF/proBDNF signaling in long-lasting synaptic plasticity

    櫻木繁雄, 冨永(吉野)恵子, 小倉明彦

    第57回日本神経化学会大会  

    発表年月: 2014年10月

  • 鏡像的なシナプス可塑性におけるTrkB・p75NTR経路の関与

    櫻木 繁雄

    第93回生命機能研究科研究交流会   (大阪) 

    発表年月: 2013年11月

  • Two opposite forms of long-lasting synaptic plasticity explained by the effects of BDNF and its precursor

    櫻木繁雄, 冨永(吉野)恵子, 小倉明彦

    第36回日本神経科学大会  

    発表年月: 2013年06月

  • 繰り返しLTP・LTD誘発後のシナプス新生・廃止現象とBDNF・proBDNFシグナリング

    櫻木繁雄

    2012年度生理学研究所研究会「神経シナプス伝達の時空間ダイナミクス」   (岡崎) 

    発表年月: 2012年11月

  • Two opposite forms of long-lasting synaptic plasticity explained by yin-yang effects of BDNF and its precursor

    Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    Society for Neuroscience 42th Annual Meeting  

    発表年月: 2012年10月

  • Involvement of the BDNF-TrkB signaling pathway in the long-lasting synaptic plasticity in hippocampal slice cultures

    櫻木繁雄, 冨永(吉野)恵子, 小倉明彦

    第35回日本神経科学学会  

    発表年月: 2012年09月

  • 切片培養での長期シナプス増強におけるBDNF放出の関与

    櫻木繁雄, 冨永(吉野)恵子, 小倉明彦

    第54回日本神経化学会大会  

    発表年月: 2011年09月

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現在担当している科目

▼全件表示

担当経験のある科目(授業)

  • 人体の仕組みと病気

    山形大学  

    2019年
    -
     
     

  • 研究室研修

    山形大学医学部  

    2018年
    -
    2019年
     

  • 生体薬理学

    山形大学医学部  

    2018年
    -
    2019年